TY - JOUR. T1 - Differential expression of rat pancreatic islet Beta-cell glucose transporter (GLUT 2), proinsulin and islet amyloid polypeptide genes after prolonged fasting, insulin-induced hypoglycaemia and dexamethasone treatment. AU - Koranyi, L.. AU - Bourey, R.. AU - Turk, J.. AU - Mueckler, M.. AU - Permutt, M. A.. PY - 1992/12/1. Y1 - 1992/12/1. N2 - The question posed by these studies was whether chronic adaptive changes in glucose-stimulated insulin secretion are accompanied by comparable changes in islet Betacell glucose transporter (GLUT 2) gene expression. Control, fasted (3-day), insulin-injected hypoglycaemic (5-day), and dexamethasone-treated (4-day) rats (n=5 for each condition), were studied. After fasting significant decrements in proinsulin mRNA/μg RNA (-32 %, p,0.05) and islet amyloid polypeptide mRNA/μg RNA (-44%, p,0.05) were observed, while there was no change in GLUT 2 mRNA/μg RNA (-13%, p,0.05). After insulin-induced hypoglycaemia, decrements in proinsulin mRNA/μg ...

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Insulin is a kind of peptide hormone which is critical for glucose homeostasis. The mature Insulin peptide is derived from Proinsulin, which includes the Insulin A and B chains connected by a peptide fragment (C-peptide). Proinsulin is processed within the endoplasmic reticulum of pancreatic beta cells into equimolar ratios of mature Insulin and C-peptide. Mouse C-peptide 1 is a single chain peptide composed of 29 amino acids, while C-peptide 2 is composed of 31 residues. C-peptide is secreted together with insulin.. The role of C-peptide has been considered to keep the best configuration to form three disulfide bonds, and has no biological activity, however, recent studies indicated that C-peptide can bind, probably, a G-protein coupling specific receptor present on the surface of endothelial cells, kidney microtubule cells and fibroblasts, resulting in activation of calcium-dependent intracellular signaling, activation of Na+-K+-ATPase, and enhancement of NO synthesis. Administration of ...

United States: P. Gottlieb, Denver, CO; J. Skyler, Miami, FL; R. Hays, Wellington, FL; F. Ovalle, Birmingham, AL; V. Aroda/R. Ratner, Washington, DC; J. Berg/M. Kipnes, San Antonio, TX; L. Zemel, Denver, CO; M. Rendell, Omaha, NE; P. Norwood, Fresno, CA; P. Raskin, Dallas, TX. Australia/New Zealand: P. Colman, Melbourne; M. Gerstman, Victoria; T. Davis, Fremantle; V. Heazlewood, Queensland; J. Baker, Auckland; P. Dunn, Hamilton; R. Scott, Christchurch; J. Krebs, Wellington. ClinicalTrials.gov registration number: NCT00453375. ...

OBJECTIVE. The aim of this study was to investigate the effect of catch-up growth occurring at different stages of childhood on glucose levels and β-cell function at 7 years of age.. METHODS. Oral glucose tolerance tests were performed on 152 7-year-old children. Anthropometric data were available from birth to 7 years of age. Children were split into catch-up, catch-down, and normal-growth groups on the basis of growth rates between birth and 1 year, birth and 5 years, and birth and 7 years. Fasting and 30- and 120-minute blood samples collected during the oral glucose tolerance tests were assayed for glucose, insulin, proinsulin, and des-31,32-proinsulin levels, and area-under-the-curve values were calculated.. RESULTS. Children with catch-up growth between birth and 5 years or birth and 7 years had greater area-under-the-curve insulin levels than the children with catch-down growth. Children with catch-up growth only between birth and 7 years exhibited higher proinsulin levels and a greater ...

Insulin resistance and pancreatic beta cell dysfunction are major contributors to the pathogenesis of diabetes. Various conditions play a role in the pathogenesis of pancreatic beta cell dysfunction and are correlated with endoplasmic reticulum (ER) stress. Pancreatic beta cells are susceptible to ER stress. Many studies have shown that increased ER stress induces pancreatic beta cell dysfunction and diabetes mellitus using genetic models of ER stress and by various stimuli. There are many reports indicating that ER stress plays an important role in the impairment of insulin biosynthesis, suggesting that reduction of ER stress could be a therapeutic target for diabetes. In this paper, we reviewed the relationship between ER stress and diabetes and how ER stress controls insulin biosynthesis.

Tight glycemic control is mandatory for the prevention and treatment of vascular complications in patients suffering from diabetes mellitus. After onset of Type 2 Diabetes, patients are usually treated with diet along with or without different combinations of oral drugs. One first-line drug class are sulfonylurea drugs that are preferably provided to patients who are not obese. The mode of action of sulfonylurea drugs is to increase beta-cell secretion, but it could be shown that they lead to deterioration of the beta-cell secretion product over time, resulting in increased proinsulin secretion. Since proinsulin is an independent cardiovascular risk factor, recent publications have demonstrated an increased risk for cardiovascular events in patients treated with sulfonylurea drugs as compared to other treatment methods.. Combination therapy of sulfonylurea drugs with glitazones has been shown to counterbalance the effect of deteriorated beta-cell secretion and to improve insulin sensitivity and ...

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The information in this video has not been evaluated by the Food & Drug Administration or any other medical body. We do not aim to diagnose, treat, cure or prevent any illness or disease. Information is shared for educational purposes only. You must consult your doctor before acting on any content on this video, especially if you are pregnant, nursing, taking medication, or have a medical condition.. ...

To our knowledge, our study is the first to comprehensively assess islet cell responsivity in people with T1D using gold-standard methods across the spectrum of detectable C-peptide production. The group with high peak C-peptide (,0.400 pmol/mL) during an MMTT exhibited lower fasting glucose (111 ± 31 mg/dL), hemoglobin A1c (6.8% ± 1.0%), and mean glucose (140 ± 25 mg/dL), and greater CGM-derived time in target range (72% ± 12%). Given that the high C-peptide group was considerably less often hyperglycemic based on CGM, the lack of difference in peripheral or hepatic insulin sensitivity across the groups supports that insulin resistance in T1D is not strongly related to hyperglycemia as suggested by others (26). The high C-peptide group was the only group who demonstrated β cell responsivity to glucose during the hyperglycemic clamp conducted during the GPA test, with measurable increases in C-peptide and proinsulin secretion. Furthermore, this group also demonstrated α cell responsivity ...

The pancreotoxicity of cyproheptadine (CPH) in rats was characterized through measurement of proinsulin and insulin levels in the pancreas as well as plasma immunoreactive insulin (IRI) and glucose levels at various times during and after drug treatment. Daily oral doses of CPH (45 mg/kg) depleted pancreatic IRI to 25% of control within 3 days. Pancreatic IRI levels showed no further decrease during the rest of a 2-week treatment period and returned to normal levels 2 days after withdrawal of the drug. Pancreatic proinsulin levels were not significantly changed by CPH treatment, and the decrease in pancreatic IRI can be ascribed primarily to a decrease in insulin. Nonfasting hyperglycemia was evident after two doses of CPH and persisted throughout the treatment period. Plasma IRI was not significantly altered compared to control and was inappropriately low for the hyperglycemia that was produced by CPH. Daily doses of CPH given i.p. (45 mg/kg) caused a transient decrease in pancreatic IRI, but ...

Disproportionate hyperproinsulinemia is one manifestation of the B-cell dysfunction observed in non-insulin-dependent diabetes mellitus (NIDDM), but it is unclear when this abnormality develops and whether it predicts the development of NIDDM. At baseline, measurements of proinsulin (PI) and immunoreactive insulin (IRI) levels were made in 87 second-generation Japanese-American men, a population at high risk for the subsequent development of NIDDM, and, by using World Health Organization criteria, subjects were categorized as having normal glucose tolerance (NGT; n = 49) or impaired glucose tolerance (IGT; n = 38). After a 5-year follow-up period, they were recategorized as NGT, IGT, or NIDDM using the same criteria. After 5 years, 16 subjects had developed NTODM, while 71 had NGT or IGT. Individuals who developed NIDDM were more obese at baseline, measured as intra-abdominal fat (IAF) area on computed tomography (P = 0.046) but did not differ in age from those who continued to have NGT or IGT. ...

Transgenic NOD mice expressing GAD antisense in β-cells have been shown to be protected from diabetes (35). However, other models in which the expression of most of the GAD sequence was disrupted have failed to show any significant difference in the incidence of spontaneous diabetes or insulitis compared with wild-type mice. This does not favor a key role of GAD in diabetes on the NOD background (45). Seemingly, disruption of the IA-2 gene in 129 mice and backcrosses of IA-2 knockout onto the NOD background allowed the role of IA-2 in the NOD mouse to be addressed. IA-2-deficient mice failed to show any difference in diabetes susceptibility when compared with wild-type mice, especially after injection of cyclophosphamide, making a key role of IA-2 in the development of the autoimmune process against β-cells unlikely (46).. We undertook a similar approach to evaluate the role of proinsulin isoforms in diabetes in the NOD mouse. We introduced a null mutation for the proinsulin 1 or proinsulin 2 ...

Susan, There a couple of answers; First, many people are more insulin resistant in the morning (part of the dawn phenomenon). This would explain your need for more insulin during the AM, both for meals and for your basal rate. Second, many people (Im told) have different insulin to carb during different times of the day. I would say that if you raise your AM basal to the point where your meal ratio is equal to the other times of the day, you will crash if you skip or delay breakfast. Just some observations that I have made. Good luck. Mario ----- Original Message ----- From: Susan Russell ,email @ redacted, To: ,email @ redacted, Sent: Tuesday, December 05, 2000 11:41 AM Subject: [IP] re: Carb to Insulin Ratio Fluctuations , For you medical buffs I need some clarification here. I am a sufferer of , varying CHO to insulin ratios throughout the day. i.e.: , , 1. Breakfast = 5 to 8 gms of CHO to 1 unit of insulin (big differences here) , (eat same toast+8 gms protein+coffee/cream almost daily) , ...

Inside the pancreas, the hormone insulin is made in the beta cells, which are part of the Islets of Langerhans. These islets also have alpha cells, which make glucagon, as well as delta cells. With each meal, beta cells release insulin to help the body use or store the blood sugar it gets from food.. In the beta cells, insulin is created first as a big molecule called proinsulin. Proinsulin is broken into two pieces: insulin and C-peptide. C-peptide is important especially when determining treatment because it can be used to measure how much insulin a person is making. The more C-peptide a person has, the more insulin they are making. This can help a provider determine how much insulin to prescribe. In people with type 1 diabetes, the pancreas no longer makes insulin. The beta cells have been destroyed and they need insulin shots to use glucose from meals.. People with type 2 diabetes make insulin, but their bodies dont respond well to it. Some people with type 2 diabetes need diabetes pills ...

Additional file 1: Table S1. of The association of diabetes mellitus and insulin treatment with expression of insulin-related proteins in breast tumors

Insulin testing may be used to help diagnose an insulinoma, and diagnose the cause of hypoglycemia in an individual with signs and symptoms Identify insulin resistance - Monitor the amount of insulin produced by the beta cells in the pancreas (endogenous); in this case, a C-peptide test may also be done. Insulin and C-peptide are produced by the body at the same rate as part of the conversion of proinsulin to insulin in the pancreas. - Determine when a type 2 diabetic might need to start taking insulin to supplement oral medications - Determine and monitor the success of an islet cell transplant intended to restore the ability to make insulin, by measuring the insulin-producing capacity.Insulin is produced by beta cells of the pancreas. It leads to Type 1 diabetes caused by Insulin deficiency & Type 2 diabetes caused by insulin resistance. This assay is useful in the management of Diabetes. It is also used for diagnosing Insulinoma when used in conjunction with Proinsulin and C-peptide ...

Importance: Detailed, nationally representative data describing high-risk populations and circumstances involved in insulin-related hypoglycemia and errors

Free resource for searching and exporting immune epitopes. Includes more than 95% of all published infectious disease, allergy, autoimmune, and transplant epitope data.

Bollheimer LC, Skelly RH, Chester MW, McGarry JD, Rhodes CJ. Chronic exposure to free fatty acid reduces pancreatic beta cell insulin content by increasing basal insulin secretion that is not compensated for by a corresponding increase in proinsulin biosynthesis translation. J Clin Invest. 1998 Mar 01; 101(5):1094-101 ...

To review, in my last post, discussing this paper, a seminal observation/conclusion can be summed up as follows: Insulin is formed in stepwise fashion from a larger protein (preproinsulin) that has a terminal signaling chain cleaved forming proinsulin that is then folded, cross-linked and has one of the three main chains cleaved in the last step(s) resulting in a protein with two parallel chains, insulin. I like this newer representation I found below because it provides the numbers in the amino acid sequence at which the cuts are made. This is important to better understanding the papers Im going to discuss here ...

GAD2 maps to chromosome 10p11.23 and encodes the 65-kDa isoform of GAD65, a major autoantigen in type 1 diabetes. The genetic variation that influences expression of preproinsulin mRNA, encoding another major autoantigen in type 1 diabetes, has already been shown to be genetically associated with disease. Previous reports that have assessed the association of GAD2 with type 1 diabetes have not used a dense map of markers surrounding the gene and have relied on very small clinical sample sizes. Consequently, no definite conclusions can be drawn from their negative results. We have therefore systematically searched all exons, the 3 untranslated region (UTR), the 5 UTR, and the 5 upstream region of GAD2, for polymorphisms in 32 white European individuals. We have genotyped these polymorphisms in a maximum of 472 U.K. type 1 diabetic affected sib pair families exhibiting linkage to type 1 diabetes on chromosome 10p and have tested both single variants and haplotypes in the GAD2 region for association

Diagnosis is based on anamnesis, examination results (including neurological examination) and registered a decline of plasma glucose in those cases where it is proved that the secretion of insulin with enhanced or not inhibitedand excluded other causes of hypoglycemia (use of hypoglycemic agents, diseases of the hypothalamic-pituitary system, adrenal lesions, hepatic failure, some other tumors).. To do this, carry out a test with fasting, investigate the secretion of proinsulin, C-peptide, cortisol.For the differential diagnosis and clarify the features may require instrumental examination (ultrasound, CT angiography).. Treatment is aimed at the normalization of plasma glucose levels.Possible subsequent surgery to remove the tumor.Patients with metastatic or ineffective surgical treatment is prescribed chemotherapy.. ...

C-Peptide, Human, 10 mg. The measurement of the C-peptide under standardized conditions provides a sensitive well accepted and clinically validated assessment of ��-cell function.

C-peptide reduces diabetes-induced glomerular hyperfiltration in diabetic patients and experimental animal models. However, the mechanisms mediating the beneficial effect of C-peptide remain unclear. We investigated whether altered renal afferent-efferent arteriole tonus or alterations in tubular Na+ transport (T(Na)) in response to C-peptide administration mediate the reduction of diabetes-induced glomerular hyperfiltration. Glomerular filtration rate, filtration fraction, total and cortical renal blood flow, total kidney O2 consumption (QO2), T(Na), fractional Na+ and Li+ excretions, and tubular free-flow and stop-flow pressures were measured in anesthetized adult male normoglycemic and streptozotocin-diabetic Sprague-Dawley rats. The specific effect of C-peptide on transport-dependent QO2 was investigated in vitro in freshly isolated proximal tubular cells. C-peptide reduced glomerular filtration rate (-24%), stop-flow pressure (-8%), and filtration fraction (-17%) exclusively in diabetic ...

Rabphilin 3a is a Rab 3-GTP binding protein concentrated on secretory vesicles of neurons and endocrine cells. There is evidence that rabphilin 3a undergoes cycles of association-dissociation with membranes and that recruitment of rabphilin 3a to secretory vesicles is mediated by Rab 3a, suggesting that rabphilin 3a is a downstream effector of this Rab. In this study we have investigated whether a membrane-anchored form of rabphilin 3a mimics the action of rabphilin 3a on secretion and bypasses the need for Rab 3 function. Overexpression of both wild-type rabphilin 3a and of a transmembrane anchored form of rabphilin 3a stimulated (about 2-fold) evoked secretion of coexpressed human proinsulin from clonal HIT-T15 cells. A similar transmembrane-anchored protein which lacked the Rab 3 binding region stimulated secretion even more effectively. Unexpectedly, a rabphilin 3a deletion mutant missing the Rab 3 binding domain was also stimulatory on secretion, although a further deletion of rab

Human insulin monoclonal antibody may be used for the analysis of the structure, function, and metabolism of insulin. This anti-insulin antibody, also known as INS antibody, is applicable for Western blot (WB) analysis under non-reducing and non-heating conditions and for immunohistological (IHC) studies of frozen tissue sections.. Antibodies to the proinsulin C-peptide (also known as insulin C) are frequently used to study the structure, function, and metabolism of insulin as well as proinsulin. Insulin C antibodies can also be used for immunocytochemistry (ICC) and for immunohistochemical (IHC) studies of paraffin-embedded or frozen tissue sections. The following insulin C antibodies are available:. ...

Human insulin monoclonal antibody may be used for the analysis of the structure, function, and metabolism of insulin. This anti-insulin antibody, also known as INS antibody, is applicable for Western blot (WB) analysis under non-reducing and non-heating conditions and for immunohistological (IHC) studies of frozen tissue sections.. Antibodies to the proinsulin C-peptide (also known as insulin C) are frequently used to study the structure, function, and metabolism of insulin as well as proinsulin. Insulin C antibodies can also be used for immunocytochemistry (ICC) and for immunohistochemical (IHC) studies of paraffin-embedded or frozen tissue sections. The following insulin C antibodies are available:. ...

TY - JOUR. T1 - Folate deficiency triggers an oxidative-nitrosative stress-mediated apoptotic cell death and impedes insulin biosynthesis in RINm5F pancreatic islet β-cells. T2 - Relevant to the pathogenesis of diabetes. AU - Hsu, Hung Chih. AU - Chiou, Jeng Fong. AU - Wang, Yu Huei. AU - Chen, Chia Hui. AU - Mau, Shin Yi. AU - Ho, Chun Te. AU - Chang, Pey Jium. AU - Liu, Tsan Zon. AU - Chen, Ching Hsein. PY - 2013/11/4. Y1 - 2013/11/4. N2 - It has been postulated that folic acid (folate) deficiency (FD) may be a risk factor for the pathogenesis of a variety of oxidative stress-triggered chronic degenerative diseases including diabetes, however, the direct evidence to lend support to this hypothesis is scanty. For this reason, we set out to study if FD can trigger the apoptotic events in an insulin-producing pancreatic RINm5F islet β cells. When these cells were cultivated under FD condition, a time-dependent growth impediment was observed and the demise of these cells was demonstrated to be ...

Simian virus 40-based plasmids that direct the synthesis of preproinsulin during short-term transfection of COS cells have been used to probe the mechanism of reinitiation by eucaryotic ribosomes. Earlier studies from several laboratories had established that the ability of ribosomes to reinitiate translation at an internal AUG codon depends on having a terminator codon in frame with the preceding AUG triplet and upstream from the intended restart site. In the present studies, the position of the upstream terminator codon relative to the preproinsulin restart site has been systematically varied. The efficiency of reinitiation progressively improved as the intercistronic sequence was lengthened. When the upstream minicistron terminated 79 nucleotides before the preproinsulin start site, the synthesis of proinsulin was as efficient as if there were no upstream AUG codons. A mechanism is postulated that might account for this result, which is somewhat surprising inasmuch as bacterial ribosomes ...

The University of Chicago (USA). The Selection Committee highly recognized that the research you have been carrying out over the years-the discovery of proinsulin and characterization of the proinsulin processing pathway, clinical applications of C-peptide radioimmunoassay for measuring endogenous insulin production, and identification of a point mutation in the insulin gene causing various abnormalities in glucose metabolism, among many other findings-has greatly contributed to our increased understanding in the mechanism of insulin secretion and related disorders.. Dr. Donald F. Steiner was therefore selected a Prize winner of 2009. ...

TY - JOUR. T1 - Polymorphism in the 5′ Flanking Region of the Human Insulin Gene. T2 - A Genetic Marker for Non-Insulin-Dependent Diabetes. AU - Rotwein, Peter S.. AU - Chirgwin, John. AU - Province, Michael. AU - Knowler, William C.. AU - Pettitt, David J.. AU - Cordell, Barbara. AU - Goodman, Howard M.. AU - Permutt, M. Alan. PY - 1983/1/13. Y1 - 1983/1/13. N2 - We sought to determine whether differences in the human insulin gene or its immediate flanking sequences could be found in diabetes. Peripheral leukocyte DNA from 217 unrelated persons, including blacks, whites, and Pima Indians, was analyzed by restriction-enzyme digestion, blotting to nitrocellulose filters, and hybridization to cloned [32P]insulin-gene probes. A region of length variation including deletions (0.1 to 0.2 kilo-base pairs) or insertions (0.6 to 5.5 kb) of DNA was found only in the immediate 5′ flanking region in 33 per cent of the genes examined. A 1.6-kb insertion accounted for 80 per cent of the polymorphism. ...

Insulin production. A. C-peptide levels in mice fed with normal chow diet (CD) and after high fat diet (HFD) challenge. B. C-peptide/Insulin ratios in mice fed

C-peptide, like the hormone insulin, is produced in the pancreas. Both are released simultaneously from the pancreas when the compound called proinsulin is split into two pieces.. Insulin is responsible for regulating the bodys glucose levels. Glucose, the bodys main source of energy, is a sugar that comes from foods.. After a meal, our bodies break down the foods we eat into glucose and other nutrients, which are then absorbed into the bloodstream from the gastrointestinal tract. Glucose levels in the blood rise after a meal and trigger the pancreas to make insulin and release it into the blood. When insulin is released, so is C-peptide.. Insulin works like a key that opens the doors to cells and allows the glucose in. Without insulin, glucose cant get into the cells and it stays in the bloodstream. The most common cause of abnormal fluctuations in blood glucose is diabetes.. C-peptide, on the other hand, has no effect on blood sugar. It is, however, useful as a marker of insulin production, ...

Summary of Facts and Submissions. I. The appeal lies from the decision of the examining division pronounced on 27 May 2010 and posted on 13 July 2010, in which European patent application 02797144.9, based on the international application published as WO 03/045316 (hereinafter: the application as filed), was refused under Article 97(2) EPC.. II. The decision of the examining division was based on the set of claims of the sole request, which was filed with letter of 20 May 2010.. This set of claims comprised 5 claims, of which independent claim 1 read as follows:. 1. A method of preparing a plasmid vector for use in a method of treating insulin dependent diabetes mellitus (IDDM) in a subject, said method comprising:. providing a DNA plasmid vector comprising a polynucleotide encoding insulin, preproinsulin, or proinsulin; and. incorporating into the vector immune modulatory sequences selected from the group consisting of 5-Purine-Pyrimidine-[X]-[Y]-Pyrimidine-Pyrimidine-3 and ...

Something goes wrong in the brain because insulin isnt signaling the way that it normally does, Galli, a coauthor of the new paper, published online June 8 in the journal PLoS Biology, said in a prepared statement. Although schizophrenia is a complex disease that is thought to have a variety of individual genetic and epigenetic causes, these researchers and others have proposed that a common thread is too little dopamine, a neurotransmitter that is involved in movement, reward and motivation ...

Does this basal profile adjustment theory wash with you guys out there or is , there simply an underlying resistance that requires and increased amount of , insulin to cover an a.m. meal?? ,, Dear Janet, My endo seems to be one of the top in the field and when I initially went on the pump he said that the average person requires twice as much insulin per carbo at breakfast than they do at the last meal of the day. I have certainly found this to be true! If I eat the exact thing at breakfast and dinner, the boluses are different. Yet if I fast through breakfast my sugars are stable, thus demonstrating my basal is on the mark. hel , , , --------------------------------------------------- , * This message was sent from Firstworld Webmail * , * http://webmail.hypercon.com/ * , --------------------------------------------------- , ---------------------------------------------------------- , for HELP or to subscribe/unsubscribe, contact: [email protected] , send a DONATION ...

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sample_1: C-peptide 6 mM; D2O 5%; H2O 95%. sample_2: C-peptide 3 mM; TFE-d2 50%; H2O 50%. sample_3: C-peptide 1.2 mM; TFE-d2 80%; H2O 20%. conditions_1: pH: 7.0; temperature: 283 K ...

The pancreatic islet of Langerhans is composed of endocrine cells producing and releasing hormones from secretory granules in response to various stimuli for maintenance of blood glucose homeostasis. In order to adapt to a variation in functional demands, these islets are capable of modulating their hormone secretion by increasing the number of endocrine cells as well as the functional response of individual cells. A failure in adaptive mechanisms will lead to inadequate blood glucose regulation and thereby to the development of diabetes. It is therefore necessary to develop tools for the assessment of both pancreatic islet mass and function, with the aim of understanding cellular regulatory mechanisms and factors guiding islet plasticity. Although most of the existing techniques rely on the use of artificial indicators, we present an imaging methodology based on intrinsic optical properties originating from mature insulin secretory granules within endocrine cells that reveals both pancreatic islet mass

Ribosomes synthesizing nascent secretory proteins are targeted to the membrane by the signal recognition particle (SRP), a small ribonucleoprotein that binds to the signal peptide as it emerges from the ribosome. SRP arrests further elongation, causing ribosomes to stack behind the arrested ribosome. Upon interaction of SRP with its receptor on the ER membrane, the translation arrest is released and the ribosome becomes bound to the ER membrane. We have examined the distribution of unattached and membrane-bound ribosomes during the translation of mRNAs encoding two secretory proteins, bovine preprolactin and rat preproinsulin I. We find that the enhancement of ribosome stacking that occurs when SRP arrests translation of these proteins is relaxed in the presence of microsomal membranes. We also demonstrate that two previously described populations of membrane-associated ribosomes, distinguished by their sensitivity to high salt or EDTA extraction, correspond to ribosomes that have synthesized ...

The gut hormone glucagon like peptide-1 (GLP-1) has been shown to have important effects on maintaining the function and health of the insulin producing beta cells. This hormone is known to increase the production rate of new insulin as well as increase the release of insulin into the blood. We will measure the rate of new insulin production in subjects with Type 2 diabetes compared to non diabetic subjects. We hypothesize that subjects with Type 2 diabetes make less insulin in response to GLP-1 compared to non diabetic subjects ...

For years an assumption was made that C-peptide, a byproduct of insulin biosynthesis, possessed no appreciable physiologic role. As other contributions in this volume amply testify, the time has come to re-evaluate that notion. C-peptide either directly through interaction with its specific cell-surface receptor or indirectly through an interaction with a related membrane entity, exerts a unique effect on several intracellular processes.We review here results of studies attempting to elucidate such molecular effects of C-peptide in different cell systems and tissues. Lacking a purified C-peptide receptor, we also demonstrate C-peptide effects on distinct elements of the insulin signal transduction pathways.

Rates of ED visits and subsequent hospitalizations for IHEs were highest in patients 80 years or older; the risks of hypoglycemic sequelae in this age group should be considered in decisions to prescribe and intensify insulin. Meal-planning misadventures and insulin product mix-ups are important tar …

K. H. Johnson, P. Westermark, G. Nilsson, K. Sletten, T. D. Obrien, D. W. Hayden, K. H. Johnson, P. Westermark, G. Nilsson, K. Sletten, D. W. Hayden, K. H. Johnson, P. Westermark, G. Nilsson, K. Sletten, D. W. Hayden ...

Human crude and recombinant interleukin 1 (IL-1) was found to dose- and time-dependently affect the biosynthesis of (pro)insulin in isolated rat islets of Langerhans. Incubation of rat islets with either 0.5 U/ml or 5 U/ml of crude IL-1 for 1 h had no detectable effect on (pro)insulin biosynthesis. …

Insulin-like growth factor-1 (IGF-1) is structurally homologous to proinsulin. IGF-1 is produced by several cell types and may have autocrine, paracrine and endocrine functions. IGF-1 is a potent mitogen that mediates the growth-promoting activities of growth hormone postnatally. It also plays a role during embryonic growth and differentiation. Recombinant mouse IGF-1 is a 7.6 kDa protein containing 70 amino acid residues. IGF-1 receptor is a disulfide-linked heterotetrameric transmembrane glycoprotein with an intracellular tyrosine kinase domain ...

A new study from the University of Florida might mean hope for the millions of people around the world diagnosed with type 2 diabetes. The findings of FSUs research, which was published in PLOS Computational Biology, indicates that there is a way to restart insulin production in the bodies of type 2 diabetics.

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